This has been on my list to talk about for some time, and I’m glad it finally came together. In this episode I cover what weight set point theory is, how our body determines our set point, and factors that could contribute to changing our set point over time.
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Chris Sandel: Welcome to Episode 114 of Real Health Radio. You can find the links talked about as part of the episode at the show notes, which is www.seven-health.com/114.
Welcome to Real Health Radio: Health advice that’s more than just about how you look. Here’s your host, Chris Sandel.
Hey everyone, welcome back to another episode of Real Health Radio. Before I start, I just want to say that the feedback on my recent episode on free will has been wonderful. Many people have got in contact and said how thought-provoking they found it, which is exactly what I was hoping for. I didn’t expect everyone to agree with me, but if we can get people thinking and challenging their thoughts, this is what I was after. If you haven’t listened to that episode yet, then please check it out and let me know your thoughts.
Something else I want to mention before getting started is that I’m currently taking on new clients. I do this twice a year. I work with clients for a period of 5 months, where we have a consult for an hour every 2 weeks. Previously I used to do one-off consults and on a consult by consult basis, but I discovered it just doesn’t actually work very well for the kinds of people that I’m working with, so I now have this manner where it’s 5 months.
I have clients all over the world, and consults are done via Skype or FaceTime or phone. I always start with a free initial chat, and this allows me to find out about your background, about what’s going on, what you’re wanting to get out of working together, and it gives me the opportunity to explain how I work with clients and what the process would look like. Basically that conversation is us discovering if we’re going to be the right fit for one another.
If you’re interested in finding out more, you can head over to www.seven-health.com/help, and there’s more details there. You can have a read through, and at the bottom of that page there’s a link to apply for the free initial chat. If you do that, I will get back to you within about 48 hours and we can arrange a time that suits both of us.
More than half the spots are already gone, so if you are struggling with your menstrual cycle, if you’re a yo-yo dieter, if you suffer with disordered eating or really any of the multitude of topics that I’ve done podcasts on before, you can head to www.seven-health.com/help and get in contact.
This week I am back with another solo episode digging into a specific topic in detail, and I’m really excited about this one. It’s something that I’ve wanted to do for a long time, I’ve had it in the back of my mind to do an episode on for a long time; I just hadn’t got around to it. But then I had an exchange with a friend, and it put it really front and center and made me start working on it.
What happened was I was playing golf with two friends a handful of weeks ago – and if you live in the UK, this may sound a little crazy at the moment. We’ve been having so much snow and wind and real-feel temperatures as low as -12, so it doesn’t sound much like golf weather. But this was actually at the start of February, before the cold snap. It wasn’t like it was warm; it was probably still in the single digits, but it was warmer than it’s been lately. This probably shows how much I’m into playing golf. Even in nearly freezing temperatures, I want to be out there.
Anyway, one of the guys I was playing with made a comment that he was currently sitting at his highest weight. I think he had been on holiday, where he’d done lots of nice eating. There might’ve been some stress leading up to that. But he was now at the higher end of things. With this, he mentioned that basically whatever he did, his weight wouldn’t go any higher – that even if he went home and just ate peaches and ice cream, things wouldn’t really change. He felt like he was at his body’s ceiling.
He then went on to mention that the opposite is also true. He’ll have times when he’s sitting at the low end of things, where he’s exercising more, he’s less stressed, he’s sleeping more, he’s eating healthier, but no matter what he does, his weight just won’t go any lower. He says that he has this band of about 6 kilos or 8 kilos – I can’t remember the exact figure that he said – which is about 13 or 17 pounds, for those who think in pounds, and that this was the difference between his highest and his lowest weight, and he just naturally moved around in this band.
What he was describing that he had noticed is something that has a lot of research to back it up. It’s a concept known as weight set point theory. This is what today’s podcast is all about.
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It’s an idea that I’d come across many years ago. It might’ve been in Linda Bacon’s book, Health at Every Size, or it was probably in a Matt Stone book or a Matt Stone article. It’s something I’ve been fascinated with ever since.
Since that fateful day on the golf course, I’ve been delving into the research around weight set point theory. I started with a search on PubMed looking for papers on the topic, and then just let things naturally spiral from there, reading papers that other articles made reference to and just following that natural process.
Gwyneth Olwyn, who runs the site EDInstitute.org, has written a lot on the topic. Her site used to be called Your Eatopia, if anyone knows it by its former name. So I went back through some of her articles on weight set point.
In the show notes, I’m going to be including all the articles and the papers that I’ve read that were relevant. Some of them I’m going to be directly referencing in this episode. But if you want to explore this topic in more detail and want to look at all the papers and articles, check out the show notes, as it’s going to be a good starting place.
Part of the reason why the weight set point theory is so fascinating is really twofold. The first is that it’s amazing that our bodies actually stay within a narrow band. We have times where we eat more, times where we eat less, but over many decades, people can stay at roughly the same place.
For example, if you ate one extra peanut a day, which is just 11 calories, and you kept this up for a decade, this would amount to an extra 40,000 calories over this time. The basic weight rhetoric is that for every extra 3,500 calories, this leads to a pound increase in weight. This kind of simple math is flawed, but if we use the example, a decade of eating just one extra peanut a day would lead to a weight gain of about 10 pounds, or 5 kilos. One peanut can, in theory, do this.
To think that something so minor over many years could lead to significant chance, and yet people can be weight steady, is incredible.
But the second part that is equally fascinating is when this doesn’t happen. If we are meant to have a weight set point that the body’s meant to keep us between, how can it be that someone is 100 pounds heavier at age 40 than when they were at 25? Or how is it that someone’s able to suffer with anorexia, where they reduce their weight drastically to the point where systems and organs are shutting down? If the body is meant to protect us and keep us in a certain weight band, how can these extremes happen?
What I want to do with today’s show is best answer these questions to explain how the weight set point works to keep someone’s weight stable over decades, and to explain that if this is meant to happen, what are the circumstances that can make this go awry?
When I say I’m going to explain or answer these questions, what I mean is I’m going to give the best explanations that they’ve come up with at this stage. Truth be told, this has actually been a difficult podcast to put together. What I’m covering under the guise of weight set point theory is actually lots of different theories. Set point theory is just one concept; there’s also settling point theory, the general model of intake regulation, there’s metabolic versus hedonic weight regulation, there’s the “Selfish Brain” theory, and so on. Lots of different theories with pros and cons that answer some questions but not others. What I’m trying to do is understand how all of these different ideas can fit together.
At times, I will be specific about one of these theories. For example, I’m going to talk about the “Selfish Brain” theory. But typically what I’m covering is going to be an amalgamation of all the different theories that I’m putting under the banner of weight set point theory. As I said, I’m going to be including all the articles I use as part of this show in the show notes, so if you want to geek out on the nuances between these different theories and different ideas, you can.
To start with, let me give an overview of what I mean when I say weight set point theory. It correlates with the story I mentioned about my friend’s experience, but let me now give the bigger picture ideas before we start drilling down to how it actually works.
The set point theory is the idea that the body naturally and automatically controls your weight. The theory suggests that the body is regulated at a predetermined or preferred level by a feedback control mechanism. Now, with the set point, this isn’t an exact number, but it is a range. Like I described with my friend, who had an upper limit and a lower limit that he typically moved between, this is what happens.
How big someone’s weight range is can really differ. For some people, it’s going to be pretty small, whereas for someone else it can be much higher. It’s often estimated at being roughly 10% to 15% of your body weight. Most people will fluctuate up and down within this range on a regular basis. However, moving out of this range is much more difficult.
I know this from myself. My set point range is probably somewhere around 6 or 7 kilos, so 13 to 15 pounds. I probably have a narrow set point in the middle of this range that I’m normally in, where it’s probably, say, 2 or 3 kilos, or 4 or 6 pounds. But if I take into consideration the times when I’m under a lot of stress and I hit my upper limit or when it’s the middle of summertime and I’m walking a ton and I’m playing multiple rounds of golf all week and I’m at the bottom end of it, it probably follows this broader range.
But with this broader range, when I hit the bottom of my range, even if I eat very little and I do a load of exercise, it doesn’t go any lower. When I hit the top of my range, no matter how much I eat, it doesn’t get any higher. Or if it does, it’s only momentarily, and I won’t spend much time at those numbers.
I’ve talked about this previously as part of an overeating experiment I did. I will link to the episode in the show notes for anyone who wants to check it out. It was Episode 40. But in short, over a period of 9 weeks, I ate just shy of an extra 35,000 calories. While my weight went up at first, it soon hit a ceiling and then started coming down. Despite averaging 3,300 calories a day, towards the end of the experiment my weight was lowering.
The opposite is also true and is why weight loss over the long term typically isn’t successful. Yes, there are completely stupid and crazy ideas that people do under the name of weight loss, but even when people follow what appears like a sane and sensible approach, weight loss doesn’t work for most long term.
People may lose weight in the short term, but when we check on them in one year’s time, a large percentage are already back to where they started. Some may even be higher than where they started. And for those that are still below where they started a year ago, they’re not as low as they were when they first lost weight. So they lost weight, they hit some low point, and now they’re on the increase. By Year 2, even more people are back to where they started. Again, those who are still lower than where they started aren’t as low as where they were at their lowest point, and they aren’t as low as where they were after Year 1.
When you just keep following this out year after year, by about Year 5 you are in a very tiny percentage of people who are still lower from where they started. Most weight loss trials don’t go on this long. Often it’s a year max. But some do follow them longer term, and with the longer term studies, the average for those people who do keep weight off longer term is about 5% to 10% reduction in weight. This is how obesity researchers typically think of weight loss success. It’s not that someone’s gone from being obese on the BMI scale and now they’re normal on the BMI scale. It’s someone who’s kept off 5% or 10% of their initial weight loss, and this is considered a success.
But if we consider set point theory and the idea that people’s weight naturally floats between a band of about 10%, all we’re looking at with these people is someone who was previously at the top end of the weight set point before the weight loss study, and now they’re sitting at the bottom end of their weight set point.
The set point, even when it’s working as it should be, will fluctuate based on age. As a child, as a teenager, weight is going up as you’re growing and developing. But once you hit a point where this growth stops in adulthood, you’ll typically be static. Adulthood here won’t necessarily just mean 18. I know for me, it probably wasn’t until my mid-twenties, even late twenties, where I’d fully filled out and stopped growing. But once someone hits this point, for the next couple of decades the set point will be fairly stable.
However, it then shifts naturally upwards between the ages of approximately 50 and 65, and women’s set point might shift a little earlier upwards because of menopause and the changes in these reproductive hormones. But this also happens with men, just maybe a little later. Then it starts to naturally shift downwards into old age.
I know we live in a society where weight gain is always seen as a bad thing – which I disagree with – and this weight gain around the fifties or sixties may have a protective mechanism. To quote Gwyneth Olwyn, this might be due to “bone and muscle density changes associated with the natural aging process that signal the necessity of a shift upwards in fat mass, nudging the optimal set point as a health protective process to ensure overall vitality into advanced old age.”
That is the basic idea of set point theory: that we all have a set point that our body is trying to keep us between, that it’s not a static number, but a range of about 10% or 15% of our weight, and that in this range, we can make changes and that if we get a little lower or if we get a little higher, the body’s more likely to be okay when we’re within this range. But once we start pushing outside of this, the body becomes more determined in making changes that push us back into the range.
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With that basic idea, let’s look at how the body actually achieves this. To answer this, there are two parts to this question. One is, how does your body know what it weighs? Or if it’s not weight specifically, what is it using as a proxy to determine if we are too high, if we’re too low, if we’re just right? Then the second part of this is if the body determines we are shifting outside of this zone, how does it rectify it? What changes does it make to move us back to a place where it feels more comfortable?
To answer the first question about how the body knows how much it weighs or what it uses as a proxy, I’m going to look at some of the research.
The original idea around set point theory – and I mean specifically weight set point theory, not in the more general way I’m using that term – is that the body uses body fat as the proxy for weight. Body fat is the gauge, it’s a thermostat that then is the set point of how the body sets the weight.
We then more recently discovered leptin. We discovered leptin as a hormone in about 1994, and this then seemed to make even more sense about body fat being the gauge. Leptin is a hormone that is produced by fat cells and communicates with the brain to regulate energy balance. As leptin goes down, you tend to increase more food, and as leptin goes up, you tend to consume less food. The idea was that as fat increased, so did leptin, and it causes more energy intake to go down, pulling someone’s weight back into their set point band. If fat decreased, leptin would also decrease and cause hunger and energy intake to go up, pushing someone back into their band.
That is the first idea. Another supposed way that the body is keeping tabs on what weight is or what it weighs is actual mass. Not specifically body fat, but total body weight. For this idea, let me touch on a couple of bits of research that have been done on rats. Yes, I know humans and rats aren’t the same things, but it can give some of an idea.
The first bit of research looked at what happens when you put a rat in a hypergravity environment. Basically the opposite of going into space, where there’s less gravity, this is what happens when you increase gravity. If you increase gravity, then the body experiences this extra pull as extra weight. So they put these rats in a hypergravity state induced by centrifusion, and the body mass of the rats decreased. They lost fat mass, their energy expenditure actually increased, and their food intake decreased. Once the weight was lost over the longer term, food intake returned to normal. In a sense, the extra gravity made the rat think it was heavier, so it lost weight.
The second bit of research involved inserting a weight into a rat. They would open them up, they’d insert a metabolically inert weight, and then sew them back up and see what happened. A similar kind of thing to the first experiment, but instead of increasing the weight by hypergravity, they were doing it by inserting the equivalent of an internal backpack filled with rocks.
What they found was that the body mass also went down. There were differences between male and female rats and they didn’t completely get back to their original set point, so they didn’t lose the exact same amount of weight as the inert weight that had been inserted into them, but weight loss did occur.
There was an interesting paper done in humans that tried to look at this, or as best they could, so they looked at African women who carried baskets on their head. These women aren’t just carrying small amounts of weight in these baskets; these baskets are carrying up to 70% of their body mass. So if they weigh 60 kilos, or 130 pounds, they’re carrying a basket that weighed 40 kilos, or 90 pounds. My mind just boggles at how this is even possible. My neck and head are sore just thinking about it. But anyway, they took these women and they then put them in a lab setting and they got them to walk on a treadmill and looked at what happened in terms of their oxygen consumption as a proxy for how much energy they were using.
What they found was that standing still, it didn’t make much of a difference. They could stand with no basket or they could stand with a basket of 60% of their body weight and it didn’t change their oxygen consumption. But when they started walking, this was when things changed. For the first 20% of the load, it made no difference, but if they added a weight that was 30% of their mass, then they would use an extra 10% of energy. If there was a weight that was 40% of mass, it would use an extra 20% of energy. It just went up in this fashion.
Now, obviously there are limitations with this study, but it can point towards mass having an impact on how the body regulates its energy use, which over the long haul would regulate someone’s weight. But more than anything, I just found this study super interesting and wanted to mention it.
Another supposed way that the body judges its weight or uses a proxy is via lean mass – not mass in total, not body fat, but lean mass. With the rat study that I mentioned earlier, when they inserted the inert weight, what they found was they actually lost fat mass, but there was a strict conservation with lean tissue. Now, if the body fat was the feedback mechanism by which the mouse determines its weight, then body fat should’ve stayed the same, and other types of tissues should’ve changed because it would look at the fat mass and realize that this is normal. But this is not what happened. It preserved the lean mass, which could point towards it being the proxy by which the body uses.
Another example of this, which again could point towards lean mass being the determiner, is the Minnesota Starvation Experiment and what happened as part of the recovery period. I’ve done a whole podcast show on this study before. I’ve actually made reference to it in lots of shows because of how important it is and because of the ethics that we can never do this again. If you want to hear all about it, then you can check out that episode. It’s Episode 42, and I’ll be linking to it in the show notes.
But as part of the experiment, after the men had been starved for 24 weeks, they’d lost approximately 25% of their body weight, which was on average 16.5 kilos or 37 pounds. Then during the recovery period, once the men were finally allowed to eat, they just unleashed. They were consuming up to 10,000 calories a day and having mixed feelings of being full but also unsatisfied and wanting to eat more.
But the part that’s relevant here is what happened with their weight. Obviously the men’s weight started to increase, but it’s the composition that’s important. After 12 weeks of eating as much as they wanted, body fat matched pre-experiment levels despite the fact that the men were still weighing less than where they started. This is common in refeeding after restriction, especially when the caloric intake is high. Fat deposits tend to increase at a faster rate than the active tissues, like muscles and organs, which have previously been broken down to be used as energy sources.
This is why in recovery from a restrictive eating disorder like anorexia, getting someone back to their pre-disorder weight isn’t where the recovery should stop, because at this stage the body still has only been prioritizing fat gain as opposed to building or rebuilding the muscle and the organs.
But back to the experiment. By 8 months of unrestricted eating, lean body mass was finally restored to pre-experiment levels, but abdominal fat was 40% higher from where they started. But it was then at this point that fat levels began to drop, despite the men eating to satiety, and this continued on. By 46 weeks of unrestricted eating, weight and fat percentage had returned to basically pre-experiment levels.
This experiment would point towards lean tissue as being the determiner of set point, and when the lean tissue hit the point the body felt comfortable, then it stopped gaining weight and the fat stores started to decrease. This is part of the reason I would propose that someone with a history of dieting notices that their weight continues to go up and up over time, because with each diet they lose both fat and lean tissue, but as part of recovery, fat is laid down first before lean tissue. But before lean tissue then hits that level where the body feels comfortable again, the person has noticed their weight’s increased, so they do another diet.
You get to a stage where someone can weigh the exact same figure now as they did 10 years ago, but they have a much lower lean mass and they have a much higher fat mass. Because of how the body interprets this, it still feels that it’s sitting at too low a set point.
Another proposed proxy for weight set point is the hormone CRH, also known as corticotrophin-releasing hormone. This comes from a paper called “Regulation and the ponderostat,” but it is referenced in other papers that I read. CRH is a stress hormone. It is released as part of our daily life, but it does increase when we are under intense stress. If stress is mild, you may get a tiny spurt of CRH to activate the stress system, but then it is quickly cleared. But if stress is intense and is ongoing, then CRH can remain high.
CRH inhibits appetite, which, from an evolutionary perspective, makes sense. The stress response is meant to get us out of a tricky situation. It takes a lot of time and resources to digest your food and convert this into energy, so if it’s an emergency, there isn’t time for you to be digesting your food. So it shuts off hunger, it shuts off digestion, and you call on the reserves of the body.
But while CRH is thought of as stress hormone, the body can also use it to regulate appetite. The paper argues that rather than the fat tissues being the determiner of weight set point, it’s really the hypothalamus, which is a section in the brain that releases the CRH.
I want to mention one more way that the body can potentially use some proxy to work out its set point, and this connects to the idea of CRH, but it does more broadly by focusing on the brain. This idea comes from a really fascinating paper called “The Selfish Brain.” I was unaware of this theory prior to putting together this podcast, and I really am grateful that I put together this podcast, that I found that paper.
It’s about 30 pages long excluding the references, so it’s not a quick read, but if you like this episode and are so inclined, I would really recommend checking it out in the show notes. It’s not light reading, but it’s worth it if you really want to understand the science.
What this proposes is that the weight set point regulation is actually determined by the energy that is making it to the brain. Our brains, despite weighing a tiny total of our weight, use around 20% of our energy, and while other tissues and organs can use a wide variety of energy types, because of the blood-brain barrier, the brain is limited in what it can use. It preferentially uses glucose, but in extreme circumstances, it can use ketones or it can use lactate.
I’m going to be coming back to this when I talk about how someone could be much heavier or much lighter than what we’d imagine with the set point, but let me just give a brief summary of the Selfish Brain theory.
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The idea is that the brain and the body are separate – not in real terms, but in terms of explaining this model. It is that the body has its energy needs and that the brain has its energy needs, but it is the brain that is controlling the show. When its energy requirements are met, that will determine the set point.
So if for some reason the system is tilted so that more energy is going to the body, then someone’s going to have to eat more food until the brain hits the point at which its needs are met. In this case, someone is going to put on more weight. Alternatively, if for some reason the system is tilted more so that energy is going to the brain preferentially, then this set point is going to be hit earlier, and so their set point or where their weight is is going to be lower.
I am completely simplifying this as part of the model. All of the other earlier components I talked about are still relevant. Feedback about body fatness or lean tissue or total mass and CRH levels, they still matter, and they’re taken into consideration. But the energy intake that is actually meeting the brain or making it to the brain is the determining factor, and this is the proxy by which the set point is set.
For me, this makes a lot of sense. Even if this model turns out to be wrong and the brain isn’t the ultimate determiner, I don’t think that there’s just one proxy that the body is using. There are going to be multiple feedback mechanisms that the body has on its dashboard when it’s trying to work out the set point.
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For example, genetics is something I haven’t mentioned yet, but someone’s genetics – which is not a proxy – has a huge impact on someone’s weight It’s estimated that between 50% and 70% of someone’s weight is genetic.
This is a tough one because it’s not like there is a skinny gene or an obesity gene, the idea that single genes are responsible for someone’s weight. This just isn’t correct. Sure, there can be single-gene mutations that can have a real impact on someone’s health, but this is rare. It’s more like a thousand genes or a hundred genes that are all doing different things that then control someone’s weight.
Then on top of this, we also know that genes aren’t set in stone. Genes are impacted on by the environment. Two people can have the same gene, but changes in the environment make it behave completely differently – how that person was raised. There is a gene and environment relationship.
But with all of that said, our genetics do have a determining impact on our set point. Some of the research that has been done to come up with that 50% to 70% figure, they use identical twins, monozygotic twins, especially twins that are separated at birth and then raised apart. If you take two people with identical genetics and then you raise them in separate environments, you see what happens.
Or you can do the same thing in the opposite direction to see what the push of the environment is. You look at a family that has some biological children and then has some adopted children, especially if those adopted children or that adopted child was adopted while very young, shortly after birth. These children, both the biological and then the adopted, all live in the exact same environment, and then we get to see what happens when they grow up.
It’s from studies like these, amongst others, that the estimation that genetics account for 50% to 70% of our weight come from. While genetics isn’t a proxy, it is something that will have an impact on our set point.
That’s it for the first question around how the body knows what it weighs or how it knows what level it wants to keep it at. There really isn’t just one answer.
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The next question, then, is how does it accomplish this? How does it cause us to put on weight when it thinks we weigh too little, or how does it get us to decrease our weight when it thinks we weigh too much? To answer this, I’m going to speak in broad terms.
I could get into the nitty-gritty details and talk about high and low-affinity ATP sensitive potassium channels in the brain and how much this affects energy making it to the brain or how the ventromedial nucleus of the hypothalamus regulates allocation while the lateral hypothalamus regulates appetite and eating behavior – but for the point of the podcast, that is way too much detail and totally pointless. It’s just not necessary. What I want to do as part of this is just talk very generally.
Very generally, our weight is determined by calories in versus calories out. And yes, I know people argue about this all the time. Is a calorie really a calorie? Do you absorb more calories from certain processed food versus whole foods, or do certain calories cause changes in the body that make us burn more or less over the long haul? Even when you consider all of these nuances and other nuances I haven’t mentioned, someone’s weight will still be determined by what is the balance of calories in versus calories out.
The way the body regulates the weight set point is therefore by impacting on how much is coming in, how much is being used, and a combination of both.
Let me spend some time just looking at what is included as part of calories in versus calories out because it’s a little more complicated than just what you eat and how much exercise you do. This section takes some of its information from the podcast I previously mentioned about my overeating experiment, and that overeating experiment podcast is by far my most-listened-to episode. If you haven’t checked it out, give it a listen.
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Let’s start, then, with the calories in. Calories in is largely dictated by the amount of food you eat. If you eat 2,000 calories, the maximum calories in is going to be 2,000. If you eat 3,000 calories, the maximum calories in is going to be 3,000.
The reason I said maximum calories is going to be 2,000 or 3,000 is because all of the calories that you eat won’t necessarily be absorbed. If your body is thinking you’re below your weight set point, it can either get us to eat more food or it can start increasing the amount that we absorbed from that food. Or it can push us more towards refined foods that are easier to digest.
It can equally do the opposite. I know for myself, if I go on holiday and I’m eating out at restaurants and I’m having more fast food, I find it enjoyable for a while, but I reach a point where I go off it. I want to have more vegetables. I want to have more foods that are higher fiber or lower calories. I want to have more fruits. So I either start eating less calorie-dense foods, or if I don’t, my body starts absorbing less. More food, more energy passes through unused and out the other side.
Let’s then look at the “calories out” side of things, which has a number of components. The first part of calories out is resting metabolic rate or basal metabolic rate. This is what the body uses each day maintaining your basic bodily functions – breathing, circulating blood, regulating temperature, growing and repairing cells. I often describe this as what your body would need if you are in a coma. Someone’s basal metabolic rate depends on their weight, depends on body composition, depends on sex, age, genetic predisposition, and possibly the bacterial population of your gut. Basal metabolic rate can really vary from person to person, so despite no more or no less effort from someone, they could need to add in a lot more or eat a lot less food each day to maintain the same weight.
Your body, depending on where it is within your set point, can decide to increase or decrease your basal metabolic rate. For example, during the Minnesota Starvation Experiment, at the end of the starvation period, the men’s basal metabolic rate had plummeted by as much as 50%.
There was an article that came out a couple of years ago by Gina Kolata in the New York Times looking at past participants of The Biggest Loser, and how so many of them struggle to keep the weight off. She looked at their basal metabolic rate and how much it had been reduced, and even though it was 6 years on, their rate had never recovered, and it was still at very low amounts.
At the other end of the spectrum, basal metabolic rate can seriously increase. There is a famous overfeeding experiment called the Vermont Prison Experiment that was conducted in 1964. There were seven prisoners who were enlisted as part of the experiment. Five were subjects, two were controls. The intention of the study was to measure the number and the size of fat cells once weight had been gained, and then compare this to the controls.
To get the men to gain weight, they had to overfeed them, and they started feeding them up to 4,000 calories a day. Weight initially went up, but then it plateaued, so they then increased their intake further, making the prisoners eat somewhere between 6,000 and 10,000 calories a day. Again, this kind of feeding led to weight gain, but not as much as would’ve been anticipated. As part of the study, they started off with the men doing rather strenuous exercise, but as time went on, they had them cease doing the exercise because they were just not gaining the weight as they hoped.
The study didn’t keep a check on all the different energy components that could’ve been accounting for why the extremely high amount of calories weren’t leading to the weight gain as quickly as anticipated, but an increase in basal metabolic rate would have been part of this.
Just as a side note, basal metabolic rate is constantly in flux. It moves up and down depending on many factors. For example, where a woman is in her cycle can affect basal metabolic rate. It actually increases as the cycle goes on, peaking and calling for the most calories the week before menstruation, before falling back down during and after the period.
The next component of the “calories out” figure is the thermic effect of eating. Digesting your food actually uses up calories, and this digestion can typically represent about 10% of the calories figures that someone takes in. But it differs depending on which macronutrient we’re talking about. Protein takes the most energy to digest, so 20% to 30% of total calories in the protein eaten is used to actually digest it. Next then is carbohydrates; 5% to 10% of the calories in carbohydrates are used as part of its digestion. Then digestion of fats is between 0% and 3%.
But this doesn’t tell the whole story. For example, fats, you apparently only need up to 3% of the calories to digest, but if you eat a tablespoon of olive oil, this is going to be very different to eating a handful of nuts, even if the two contain the exact same amount of fat calories. Or the ability to get protein out of a chicken breast or some eggs will be very different from your ability to get it out of lentils. It’s not just the macronutrients that affect digestion, but the types of food.
But again, this thermic effect of eating is under some level of body control. How much the body wants to spend on digestion can be affected by where someone is within their set point.
The final two categories of the “calories out” equation relate to movement. The first is known as non-exercise activity thermogenesis, or NEAT, and these are all the non-exercise movements that we do during our day. Think of all the movements that are fundamentally part of our day-to-day life, or at least were fundamentally part of it before all the labor-saving devices we now have – walking, standing, gardening, washing dishes, hanging clothes out on the line, typing, showering, fidgeting, etc. Again, NEAT is something that is controlled by where we are on our set point. When people restrict their calorie intakes, we start to see a reduction in their NEAT. This might not happen immediately, but the more someone is pushing outside of their set point and there’s that reduction in energy, the more the body wants to reduce its out point.
The same happens in the opposite direction, with an increase in NEAT. There was a study conducted at the Mayo Clinic, and as part of this, researchers overfed 16 normal-weight subjects by 1,000 calories a day for 8 weeks, and as part of this, they asked them not to perform any purposeful exercise. They wanted to see what would happen.
Despite consuming an extra 1,000 calories a day, what the participants actually gained in weight varied massively. I think this is a perfect illustration of set point theory and how individual our bodies are with weight. It’s the bodies making the choice of what happens in response to this food.
What should’ve happened with an increase calorie amount of this nature – and this is if we believe the calorie math – is that these subjects should’ve gained about 16 pounds, or 7 kilos. The person who gained the least only gained 0.79 of a pound, or 350 grams. So despite eating an extra 1,000 calories a day for 8 weeks, they gained less than a pound. The person who gained the most gained 9.3 pounds, or 4.2 kilos, and everyone else was in between. Quite a spread.
Interestingly, they kept check on the metabolic rate, on the thermic effect of food, and physical activity, and while these things changed, it wasn’t anything in comparison to what happened with NEAT. For example, the highest person had their NEAT change by 692 calories a day. Despite being told not to do any physical activity, this person naturally started to move and stand and fidget more to the tune of 692 calories. This is a huge amount of calories to be used for minimal movement. That was the highest, but the average was that NEAT increased by 336 calories per day.
This movement, whether we’re talking about the NEAT increasing or the NEAT decreasing, is largely subconscious. These people aren’t actively thinking “I need to move more” or “I need to move less.” It just starts happening.
The final realm of “calories out” is physical activity. This is exercise in the way that most people typically think of exercise. It’s going for a run, going for a swim, lifting weights, playing tennis, doing rock climbing – choose your exercise. What happens here is the body can push someone to do more or less time total physical activity, or during the time that someone is doing physical activity, it can choose to use more or less energy during the session.
Say the body feels like there is an abundance or an excess of energy, so you go for a run. You may find that you run for a longer period, or during your normal running period, you’re able to run better and you do a personal best for your average minutes per mile or minutes per kilometer. I am simplifying things here for illustrative purposes, but this is how the body can increase its physical activity output.
The same is true in reverse. You may have a terrible run and feel like stopping early, or you are much slower and you feel like you just don’t have the energy, because your body is wanting to lose less.
Let me just give an example of how exercise doesn’t always have the impact that we typically think it would. We would assume that if someone goes from no exercise to exercising regularly, obviously calories out have increased and weight loss will ensue.
This was a study done by John Berardi from Precision Nutrition. It was done at the University of Texas. They took 100 people; 50 were the subjects, 50 were the control, and all of these people were sedentary. The subjects were then given an exercise program to follow. They went from no exercise to exercising between 5.5 and 6 hours a week. This included three weight sessions and two group interval sessions, and they did this for 12 weeks. Then you had a control group, and they just did nothing.
At the end of the 12 weeks, the average weight of the subjects who were doing the exercise was that they weighed 1 pound more. No, I didn’t just misspeak; they went up. They had in fact lost some fat, 1 pound’s worth, and then they’d put on lean tissue, 2 pounds’ worth, and this accounted for the slight increase in weight. But for 12 weeks of hard training of 5.5 to 6 hours a week, this is a pretty minuscule change in body composition. For the control subjects, weight stayed the same.
This just goes to show the compensatory mechanism that is often at play. If you pull one lever, the body pushes another one and vice versa.
For me, another perfect example of the weight set point in action was my partner Ali’s pregnancy. During her pregnancy, a “normal” amount of weight to put on is estimated between 10 kilos at the low end and 18 kilos at the high end. That’s around 25 pounds to 40 pounds. Ali, during pregnancy, gained 25 kilos, which is 55 pounds, so much higher than the average. While she definitely had more food in that first trimester – a lot of mac and cheese – after this, her eating didn’t change much from normal. She normally eats a lot of food but is weight steady. Then, over the space of pregnancy, despite eating what she would normally eat outside of that first trimester, her weight significantly increased. We are now five and a half months on, and Ali’s weight is basically back to her pre-pregnancy weight.
For me, this was such a perfect example of the body choosing what it wanted to do with the food that was given to it. The body regulated its set point based on what it needed to do, which was create a human, and now the set point has been re-regulated based on what it needs to do now.
So far, I’ve explained how the weight set point works in what we think of as “normal” circumstances. What I mean by this is when someone lives their life, deals with normal stress and strains, and their body weight naturally floats in a band. Sometimes it’s a little higher, sometimes it’s a little lower, but overall it stays in a range of about 10% to 15% of total weight.
00:50:05
Let me now then attempt to answer, how can people find themselves at a much different weight than we would imagine if they were meant to be contained within a set point?
Before I dig into this, let me just preface this by saying body diversity is a real thing. We aren’t all meant to be one shape or one size. People can be in the obese category on the BMI scale and be very healthy. People can be in the normal category on the BMI scale and be incredibly unhealthy. What I’m going to be covering here does not negate this. There can be reasons that the body increases the weight that are healthy and normal, and there can be reasons that the body increases the weight where it’s part of a disease process.
I’m trying to present as best I can what I can make out from the research around this topic. For me, people thinking in absolutes, whether that be that being in a heavier body is always a problem or that being in a heavier body is never a problem, I don’t agree with those absolutes. With that disclaimer out of the way, let’s look at this.
The first explanation about how someone’s weight can increase above what we would think of as their weight set point comes from a paper called “Metabolic versus hedonic obesity: a conceptual distinction and its clinical implications.” I’m definitely not a fan of the term “hedonic obesity,” so I’ll use it sparingly and I’ll explain what it means.
The paper has some similarities to the Selfish Brain in that it breaks things down between the body and the brain, but it does it differently. It looks at the fact that there is a body set point, but it believes that this set point isn’t so set in stone, but that outside of whatever the way the body uses to determine its weight, there is also a second system that impacts on eating, and that this is the hedonic system.
Hedonic comes from the term “hedonism.” It means pleasure and happiness. This is the idea that if food is more palatable and more pleasurable, we’ll eat more of it and increase our set point.
Let’s understand what is meant by pleasurable or palatable or enjoyable. While someone is eating, they might not necessarily use these terms, but this is how the food is interpreted as part of the reward circuitries in the brain. They get an increased reward from the food. This idea is that if you take someone and you give them a normal meal with fresh fruits and vegetables, their body will tell them that they’re full at say 700 calories, just to use a calorie figure. But if you then give them a meal that is highly palatable food, that is rewarding, some kind of fast food, they don’t get that full feeling until say 1,000 calories. Or even if they get that full feeling, they continue to eat more because of the reward that they’re getting.
Under the traditional weight set point model, having more food at a meal is completely normal. Weight set point isn’t determined on a meal by meal basis, but is about looking at the medium, the longer term. But what should happen is that after many meals like this, especially if weight is continuing to go up, there should be a feedback mechanism that drives someone towards eating less.
But because of the hedonic reward from food, this overrides the set point and allows it to keep increasing, so when someone sits down to the next meal, there isn’t the feedback to eat less.
This model seems to make sense in terms of the increase in weight that has occurred in tandem with changes in our food supply. As diets have increased in the amount of ultra-processed foods that are highly palatable, so has weight.
But this is just one factor, and it seems to affect people differently. For example, when I participated in my overeating experiment, I was eating lots of processed foods as this was the only way I could get in the prerequisite amount of calories, but I still hit a ceiling where I wanted to stop eating the stuff. Part of this could be linked to how someone thinks and feels about food. As part of this model, it’s the reward circuitry that is driving and overriding the set point.
If you create a situation where someone has dieted and they have this whole emotional connection to good foods and bad foods and forbidden foods, the reward someone gets from eating some ice cream or some pizza is going to be completely different from someone who simply sees this as food and has no emotional attachment.
I’ve seen this with clients, where they would describe themselves as addicted to certain foods and that they felt that whenever they ate them, they overate them and they couldn’t stop. But yet once we worked on their relationship with food, these highly palatable foods lost their power. They weren’t so interested in them.
And it doesn’t just have to be someone’s belief about forbidden food or a reaction to dieting. It can be any situation in which food is providing someone with a powerful way to change their emotional state. For example, if you are struggling to keep the lights on, to pay the rent or the mortgage, if you’re unsure if you’re going to get made redundant, if you’re in an unhappy relationship, the reward value that you get from food could be significantly heightened. Food is a way of chilling out or numbing out.
You then take someone in a different situation, where life is going much better or it’s easier for them, where they have many more coping skills or they have many more happy experiences in their life, and this food isn’t providing the same reward value. This is why we often see that thinness and fatness occur along socioeconomic lines.
I do think that a lot of talk around food is alarmist, that “sugar is as addictive as cocaine” is alarmist, and the obsession with clean eating and avoiding anything that is “unnatural.” But from my perspective, there is no denying that there is a connection between the changes in the food landscape and changes in the weight set point. While people supposedly have the ability to make decisions, and McDonald’s and Krispy Kreme don’t have a gun at your head, forcing you to eat this food, blaming the individual isn’t the solution. We are products of our environment, and if our environment is filled with this kind of food, the likelihood is people will eat more of it.
I don’t know what the solution is here. I’m not suggesting that there is an easy fix. But what I do know is that if nothing changes and we simply continue to blame the individual, at the population level, weight set points will continue to rise.
The next reason for weight set point increasing is something I’ve touched on, which is dieting. People who diet typically end up at a higher weight from where they started. There is this belief that weight cycling – the losing and the regaining and then the losing and the regaining – increases someone’s weight set point over time.
When we look at the Minnesota Starvation Experiment, while weight after the extreme dieting or the starvation did increase, once lean tissue was restored and if the men continued to eat to satiety, their weight came back down. So maybe dieting doesn’t cause a permanent shift in someone’s weight set point, but because people continue to diet again and again prior to lean tissue being restored, they never reach a point at which the body starts to naturally lose weight.
The other part of this then relates to the idea I just mentioned about hedonic effects of food. Dieting typically ramps up the reward process that someone gets from eating. Rarely do people work on this area. Instead, they just jump from diet to diet. I know for many clients that I’ve worked with with restrictive eating disorders that where they eventually settle is back to where they started. So yes, they may have some time of being higher or their weight seems so much more than where they were at their lowest, but it’s very common once all their work is done for someone to comment that they are now back in the body that they always had before their eating issues, that they now know that this is where their body likes to be.
In real terms, dieting seems to be the best predictor we have for future weight gain – but is this because of permanent changes in someone’s weight set point, or is it because people don’t ever deal with their relationship with food or get their lean tissue status back to where it was and where it should be before just going on another diet?
I will just say, please don’t misconstrue what I’ve just said here to mean that once you heal your relationship with food, the weight will simply drop off. There are lots of people that are selling intuitive eating for weight loss or similar ideas. As I always say when working with clients, I don’t know what will happen with your weight. Yes, you can make changes, but how your body chooses to react to these changes is up to your body. All I’m trying to point out is that maybe dieting doesn’t permanently increase someone’s weight set point, but it appears to if that damage isn’t repaired by lean tissue being restored and someone’s relationship with food being repaired.
There are other changes in our modern life that seem to allow the weight set point to increase. It’s becoming more widely known about the issues with light in the evening times, especially blue light in the evening times, coming from things like TVs and laptops and tablets and phones and even just normal indoor lighting, and how this can negatively impact on our health.
I’m going to quote from Gwyneth Olwyn here. She says, “The correlation between the introduction of artificial light at night and increases in population BMI are well known. Several assessments confirm nighttime lights cause a role in generating metabolic deviations that result in adipose organ enlargement as well as disease states, all with no accompanying excess intake of energy.”
I want to focus on the last bit that she said, which is “all with no accompanying excess intake of energy.” So often when we think of increases in someone’s weight or their weight set point, it’s because we believe that someone must’ve eaten more food. But as I went through previously, there’s both the energy in and the energy out component. Even without changes in total calories, changes in the environment can cause the body to use less energy and to store more of it.
The reason that artificial light seems to negatively impact weight set point probably has something to do with affecting circadian rhythm. There are many things that can also negatively affect circadian rhythm. People getting inadequate sleep negatively affects circadian rhythm and has been connected with increased weight set point. Sometimes this is linked to turning down energy usage, as I talked about with light. But poor sleep also affects hormones that regulate hunger and regulate the kinds of foods that people crave, so poor sleep can actually lead to an increase in consumption.
Lack of movement also affects circadian rhythm. When people think of movement, they typically think of the calories that are burnt from that movement, but this is only part of it. Movement during the daytime helps to entrain the circadian rhythm, and it lets it know that it’s daytime, which then at nighttime has a positive knock-on effect of helping someone to be able to sleep properly (as long as this isn’t ruined by artificial light).
So really, anything that disrupts circadian rhythm, whether that be artificial light, inadequate sleep, lack of daytime movement, doing shift work, regularly flying and being in different time zones – all of these things negatively impact on circadian rhythm and tend to increase the weight set point.
The next reason that set point can change and for many seems to have a much easier time increasing is due to evolution. Again, this is a proposed theory, but there seems to be some genetics that we can point towards to actually back this up. A part of this idea is that the body defends weight loss differently to defending weight gain. From an evolutionary perspective, it’s only been the tiniest fraction of our existence that food has been in abundance and easy to come by. For the rest of human civilization and human evolution, finding food was a daily struggle and more of a daily challenge.
The idea is that it makes sense that the body defends against weight loss much harder because weight loss is, in historical terms, potential starvation. So the body wants to have mechanisms in place that get you out there looking for food and ways it can then turn down functions so you’re losing less.
But at the other end of the spectrum, there wasn’t often a problem of overconsumption. It’s hard to overeat when your diet consists of tubers and whatever animals you’ve been able to kill. This is both because of the scarcity of this food, but also, the palatability / reward is much lower with these foods than with modern foods.
There are two parts to this theory that I also think are worth mentioning. The first is to do with where we sit on the food chain. I’m going to quote an article that this comes from, and the article is called “Set points, settling points, and some alternative models: theoretical opinions to understand how genes and environments combine to regulate body adiposity.”
The article says, “It’s been suggested, based on numerous small animal studies, that the upper intervention point in most animals is probably regulated by the risk of predation,” so the risk of dying or being eaten by something else. “In humans, who developed tools and weapons, discovered fire, and became social animals about two million years ago (Homo erectus), the risk of predation was effectively eliminated.”
Effectively, because we are sitting at the top of the food chain and are less reliant on our physical bodies to save us every day from being eaten, the upper limit is less important than the lower limit in comparison to basically all other animals.
The other part of this – and this makes sense historically as well – is that someone who could get by on less food and who was thriftier was likelier to fair better. Over time, the genetics for this became more prominent. To quote the article again, “Some individuals have been lucky in the mutation lottery and can still regulate their weight and adiposity because the upper intervention point has not been moved, but for others the intervention point has drifted upwards, and the strong control preventing weight increase is no longer present.”
I want to connect this with the overfeeding studies I mentioned before because it looks like these issues here contradict one another. It would be easy to say, “What about those overfeeding studies? Clearly people hit a set point and then came back down the other side.”
But with all of the overfeeding studies I’ve mentioned – my own personal overfeeding study, the Vermont Prison Experiment, and the experiment for the Mayo Clinic where they were eating an extra 1,000 calories a day, even for the Minnesota Starvation Experiment, which kind of turned into an overfeeding experiment once the starvation part was over and the guys were eating up to 10,000 calories a day – in all of these examples, the subjects were young men who were all lean, who had never inhabited a heavy body. It’s people who were naturally thin and physically and mentally fit.
Just because this is what happens in this population segment when they overeat, doesn’t mean that that is what happens when everyone overeats. I know personally that I sit at the extreme end of the spectrum with my difficulty putting on weight irrespective of what I do with my eating. But it would be delusional of me to think that this is the same for everyone.
I think that there is validity in this idea that people defend weight loss very differently to defending weight gain, and that this can be because of different genetics, and it can be because of different factors that make this so.
But I would also say that it’s more likely that this is then impacted upon because of other factors. If someone has a tendency to be less defensive of that upper limit so they can gain more weight, if you combine this with then lots of highly palatable food, lots of dieting, lots of poor sleep, then their outcomes are going to be much more pronounced than someone with those same genetics but isn’t doing any of those things.
The next factor that seems to override the weight set point is trauma. I’ve done a whole podcast previously on the Adverse Childhood Experiment Study, also known as the ACE Study. It’s Episode 85. I highly recommend checking it out. But to give an overview, the ACE study was orchestrated by Vincent Felitti and the medical company Kaiser Permanente. It was to do a much bigger study that looked at the work that Felitti had already started. Felitti was running a preventative medicine department, and one part of the department was an obesity clinic. It was for people who wanted to shed as little as 30 pounds, but was really a clinic designed for people who were, as they describe, 100 to 600 pounds overweight.
Throughout the ’80s, the obesity clinic had a 50% dropout rate. When Felitti looked at the dropout records, something was off. The people who were dropping out weren’t doing so because their weight had plateaued or because they were struggling with weight coming back on; they were dropping out when they were 50 pounds, 100 pounds, 200 pounds down from where they started and they were still losing.
01:09:00
Felitti brought back in some of these people who had dropped out and started asking them questions. What he found out was that a very high percentage of them had been victims of sexual abuse or incest. This then led on to the ACE Study, which then looked at around 19,000 people, and it expanded out, not just talking about sexual abuse, but a whole range of traumatic childhood experiences, from physical abuse through to a parent going to jail or a parent suffering from addiction or mental health issues.
As I talk about in the podcast, the connection between trauma and adverse outcomes in adulthood is profound. Also, it’s much more common than people think. For example, there was an estimation previously that incest happened with about 1 in a million people, or 1 in 1.5 million people; with the ACE Study, it turned out to be much, much more frequent and common than this. But because of this being such a taboo topic, and in the same way of many traumas that are asked about in the ACE Study being taboo, we just don’t talk about them, so we assume that they’re not happening.
Trauma can have a huge impact on someone’s weight and on weight set point, and this can happen in a couple of ways. It can lead to an increase in the reward response someone gets from food, which I’ve already talked about. Food becomes someone’s coping mechanism and it has that hedonic response.
The second area is using food to change body size as a protective mechanism. As one of Felitti’s patients commented, “Overweight is overlooked, and that’s the way I need to be.” Another noted that she had been abused by a number of people from age 4 onwards. She then married a man who abused her until she finally escaped, and now, every time she lost weight and a man would comment on her beauty, she’d become absolutely terrified and start eating excessively again until her weight returned.
But it isn’t always an increase in the set point, and the opposite can also happen. Anorexia and restrictive eating happens or can happen in response to trauma. I know that some people talk about suffering sexual abuse in their teens while they’re going through puberty, and then there’s this association with growing up and the development of secondary sexual characteristics and linking that with the trauma. So the reason then for the anorexia or the starvation is to become androgynous and childlike. This is the type of body that is then going to be a protective mechanism.
I know both of these examples that I’ve given here are around sexual abuse, but this is trauma in general. Trauma, in general, can affect someone’s set point, and often it is not conscious. It’s not like I’m describing here where someone is consciously doing this; it just starts to happen.
I’m currently reading the book The Body Keeps the Score by Bessel van der Kolk, which is all about trauma, and a big part of the book is how often people don’t remember the trauma that is stored in the body. It affects how the brain works, but people only realize decades later that something happened to them – which seems odd on the surface. We think, how could you not remember something like this happening? But he talks about the different brain regions and the mechanisms and why this would be the case.
So trauma is definitely a factor, and it’s something I’m planning on doing another podcast on as well. In the podcast I did on the ACE Study, I really just presented the outcomes of the study, but I didn’t have any solutions. As I said, I’m currently reading The Body Keeps the Score by Bessel van der Kolk. I have sitting on my shelf Dr. Gabor Mate’s When the Body Says No, and in my Amazon cart is Peter Levine’s Waking the Tiger. All of these books look at trauma and how to fix the body, and they all recommend solutions for dealing with it. Once I’ve read these books and delved more into the research, I will be back with another podcast on the topic.
The next factor I want to mention is chronic stress. This could be also thought of as trauma. You have, say, capital ‘T’ Trauma, which is the stuff I mentioned during the ACE Study, and then you have little ‘t’ trauma, which is more of the ongoing stresses. This can be because stress encourages all of the other factors I’ve mentioned. It messes with sleep, it drives people to comfort-eat or people to diet as a false sense of control. But stress even outside of these factors can increase weight set point. Again, this is often why thinness and fatness happen along socioeconomic lines.
Life is meant to be stressful. I don’t want to have some idyllic view of what it used to be like for our ancestors, that they had it so easy, but our modern life is now so hard. But stress previously was different. It was short-lived. There was a physical response to it. Someone actually ran or fought or dealt with the stress in some active way. They weren’t just sitting in a car having a huge stress response because they’re in traffic, or they weren’t constantly worrying about how they were going to pay their mortgage or having increased stress hormones at midnight because they were watching a screen.
This is a stress that we didn’t evolve with, and for various reasons, it then leads to the storage of more fat instead of food being used for energy, and to the increasing of the weight set point.
There’s one more reason that I want to mention for why someone’s weight point can change, and this reason is diseases. Various diseases can cause the body to regulate at different set points. This increase in weight is often the way the body is coping with that disease or that issue. Typically we blame the weight for the disease, like believing the poor habits lead to the weight increasing, and this then leads to the disease. But often what is happening is that the disease process starts, and then the change in weight is part of the body’s mechanism for either dealing with the disease, or it’s a ramification of the disease.
There is a great TED Talk by Peter Attia that I’m going to link to in the show notes. Attia talked about obesity and diabetes. We typically focus on obesity being the cause of diabetes, but as part of the talk, Attia explains that the problem starts earlier, before the weight gain, and the weight gain is secondary. Simply getting someone to lose weight may work short-term, but over the long haul it doesn’t, because the disease mechanism is still going on, so the body will continue to deal with it in the same way, which is increasing weight.
This idea is also explained in the Selfish Brain paper, although with more of a brain focus. They propose the idea that diabetes is a brain disease, and that there are two phases to it, and that preceding these phases, there is some stress or some trauma that leads to a shift in brain function.
In the first phase, the brain competes too little with the body for glucose. Even though the brain needs to hit a certain level of glucose, because more energy is going to the body first, it then takes more total calories to give the brain what it needs. This leads to an increase in weight, and because more adipose tissue mass is accumulating, that mass is then able to absorb more glucose, and this now represents a larger competitor to the brain for energy resources.
Then in the second phase, the brain starts to fight back and wants to prevent against further weight gain. More glucose then goes to the brain, but the brain also makes changes so that glucose isn’t then being taken up by the muscles and isn’t being taken up by the peripheral tissues. Hence the elevated blood sugar levels, and then the nerve damage, and then all the issues that are associated with diabetes. Therefore, Type II diabetes is a safeguard for the brain to allow it to get the glucose it needs rather than it going to other tissues.
In this theory, it’s not so much about the weight set point. Someone’s weight set point is just naturally increasing as a byproduct. It’s really about the amount of glucose making it to the brain and how tightly this is regulated for the glucose that is allowed for the rest of the body.
Then the opposite situation of Type II diabetes happens with anorexia. Again, I’m quoting from the Selfish Brain paper and the Selfish Brain model. In this model, anorexia, again, is preceded by some stress that, again, causes some changes in brain regulation. But in this instance, the stressor causes the brain to be much more militant with taking up glucose preferentially, and even in the face of restrictive eating or overtraining, the brain is still getting all the glucose that it needs while the body suffers. But because the brain is getting the energy it needs, people feel alert, they feel in control, and it can be reaffirming that there isn’t a problem with what they’re doing.
I’m massively simplifying things, both with the Type II diabetes and with the anorexia explanation. The paper goes through all of the different mechanisms and hormones and brain regions and how all of this works. As I said earlier, if you’re really interested in this stuff, then check it out. But this paper makes a lot of sense to me in explaining both how the set point works when it works, and how it can go awry when it doesn’t.
That’s it for the different reasons why someone’s weight set point could be different to how we would imagine. As always, I know I’m going to finish up recording this and then over the next couple of weeks, find other things that I wish I could’ve included. But this is what I’ve come up with so far.
I know that this is a long episode. It definitely took a long time for me to put together. I’ve learned a ton from doing it, so I’m really glad that I spent the time. It’s definitely showed me that the way that most people talk about weight set point is too narrow, and that if you just look at overfeeding studies, or if you just look at the classic set point idea that our set point is regulated by our fat stores, you’re likely going to have an incomplete understanding.
01:19:55
How I want to close out this show is with a suggestion, and my suggestion is be aware of the post-hoc stories you create about why you weigh what you do or why someone else weighs what they do, because typically we look at the outcome and then we tailor our narrative or remember facts that would help explain this.
For example, if you stood on a set of scales and it said that your number was lower than usual, it’s easy to start to focus on all of the reasons why this would be so. You tell yourself, oh yeah, you’ve started doing more walking, that you’ve been putting in an effort to get to bed earlier, that you’ve started cooking more of your own food, so these are the reasons why your weight’s then gone down.
But imagine the next day, you then found out that the scale was actually malfunctioning. Rather than having lost weight, you’ve actually put weight on. Now it’s time to come up with another collection of stories.
On second thought, you haven’t been doing as much walking as you remember, and when was the last time you did any other exercise? Yes, you’ve been trying to get to bed earlier, but you haven’t been that successful. Sometimes you’re cooking your food, but now you start to remember all those occasions that you had a meal at a restaurant or you’ve been eating a takeaway. This then becomes why your weight has increased.
We create stories to fit the outcome, but there’s nothing to say that this story is true. You don’t know what is going on in someone else’s life and how their body is functioning, and even within your own life, you don’t know why your body is doing what it does. By all means, look at the causes that can lead to an altered set point, but just realize that the explanation that you come up with might not be the real reason.
That is it for this show. I plan to do another one of these new solo shows in about a month’s time, but there will be another guest episode, and there will be other rebroadcast episodes before then.
I said at the start I’m currently taking on new clients, so if you’re interested in finding out more, you can simply head to www.seven-health.com/help. As always, thank you so much for spending your time and listening to this. I look forward to catching up with you again soon.
Thanks for listening to Real Health Radio. If you are interested in more details, you can find them at the Seven Health website. That’s www.seven-health.com.
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